The intestinal lumen is massively colonized by bacteria and for most metazoans this relationship is mutually beneficial (Ley, R. E., et al. (2006). Cell 124, 837-848). Prokaryotes productively partner with their eukaryotic hosts to aid in the digestion and extraction of energy and nutrients from food, and non-pathogenic bacteria suppress pathogenic species (Backhed, F., et al. (2005). Science 307, 1915-1920; Rakoff-Nahoum, S., and Medzhitov, R. (2006). Curr Top Microbiol Immunol 308, 1-18). An epithelial cell barrier is essential for this symbiosis as it creates a boundary necessary for coexistence by preventing mucosal inflammation in response to bacterial or other luminal stimuli (Nieuwenhuis, E. E., and Blumberg, R. S. (2006). Adv Exp Med Biol 579, 108-116; Weber, C. R., and Turner, J. R. (2007). Gut 56, 6-8). However, in some individuals this balance is upset, resulting in persistent intestinal inflammation, that manifests as the two distinct clinical entities of inflammatory bowel disease, Crohn's disease and ulcerative colitis (UC) (Boone, D. L., and Ma, A. (2003). J Clin Invest 111, 1284-1286; Rakoff-Nahoum, S., and Medzhitov, R. (2006). Curr Top Microbiol Immunol 308, 1-18; Rakoff-Nahoum, S., and Medzhitov, R. (2006). Curr Top Microbiol Immunol 308, 1-18). Determining the factors that regulate these complex host-commensal relationships and promote the development of colitis is of great clinical import and scientific interest.